NDLI: Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo.

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Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo.

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Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bell, Michael P. Pease, Larry R. Marler, Ronald J. Nava-Parada, Pilar Felts, Sara J. Cabrera, Rosalyn Schenk, Erin L. Van Keulen, Virginia P. Radhakrishnan, Suresh
Description	Country affiliation: United States Author Affiliation: Radhakrishnan S ( Department of Immunology, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.)
Abstract	Lymphocyte differentiation from naive CD4(+) T cells into mature Th1, Th2, Th17, or T regulatory cell (Treg) phenotypes has been considered end stage in character. In this study, we demonstrate that dendritic cells (DCs) activated with a novel immune modulator B7-DC XAb (DC(XAb)) can reprogram Tregs into T effector cells. Down-regulation of FoxP3 expression after either in vitro or in vivo Treg-DC(XAb) interaction is Ag-specific, IL-6-dependent, and results in the functional reprogramming of the mature T cell phenotype. The reprogrammed Tregs cease to express IL-10 and TGFbeta, fail to suppress T cell responses, and gain the ability to produce IFN-gamma, IL-17, and TNF-alpha. The ability of IL-6(+) DC(XAb) and the inability of IL-6(-/-) DC(XAb) vaccines to protect animals from lethal melanoma suggest that exogenously modulated DC can reprogram host Tregs. In support of this hypothesis and as a test for Ag specificity, transfer of DC(XAb) into RIP-OVA mice causes a break in immune tolerance, inducing diabetes. Conversely, adoptive transfer of reprogrammed Tregs but not similarly treated CD25(-) T cells into naive RIP-OVA mice is also sufficient to cause autoimmune diabetes. Yet, treatment of normal mice with B7-DC XAb fails to elicit generalized autoimmunity. The finding that mature Tregs can be reprogrammed into competent effector cells provides new insights into the plasticity of T cell lineage, underscores the importance of DC-T cell interaction in balancing immunity with tolerance, points to Tregs as a reservoir of autoimmune effectors, and defines a new approach for breaking tolerance to self Ags as a strategy for cancer immunotherapy.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	5
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antibodies Pharmacology Antigens, Cd80 Immunology Autoimmunity Drug Effects Forkhead Transcription Factors Interleukin-17 Biosynthesis T-lymphocytes, Regulatory Cytology Animals Cell Communication Cytokines Dendritic Cells Immune Tolerance Mice Multiple Myeloma Therapy Programmed Cell Death 1 Ligand 2 Protein T-cell Antigen Receptor Specificity Vaccines Research Support, N.i.h., Extramural Retracted Publication Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo. : Retraction

Reprogrammed FoxP3+ T Regulatory Cells Become IL-17+ Antigen-Specific Autoimmune Effectors in Vitro and In Vivo1

CTLA-4 control over Foxp3+ regulatory T cell function.

CD28-CD80 interactions control regulatory T cell motility and immunological synapse formation.

Allogeneic Mature Human Dendritic Cells Generate Superior Alloreactive Regulatory T Cells in the Presence of IL-15.

Dendritic cells as controllers of antigen-specific Foxp3+ regulatory T cells.

Id1 expression promotes T regulatory cell differentiation by facilitating TCR costimulation.

Plasmacytoid dendritic cells and type 1 interferon promote peripheral expansion of forkhead box protein 3+ regulatory T cells specific for the ubiquitous RNA-binding nuclear antigen La/Sjögren's syndrome (SS)-B

Convergent and divergent effects of costimulatory molecules in conventional and regulatory CD4+ T cells.

Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo.

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Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo. : Retraction

Reprogrammed FoxP3+ T Regulatory Cells Become IL-17+ Antigen-Specific Autoimmune Effectors in Vitro and In Vivo1

CTLA-4 control over Foxp3+ regulatory T cell function.

CD28-CD80 interactions control regulatory T cell motility and immunological synapse formation.

Allogeneic Mature Human Dendritic Cells Generate Superior Alloreactive Regulatory T Cells in the Presence of IL-15.

Dendritic cells as controllers of antigen-specific Foxp3+ regulatory T cells.

Id1 expression promotes T regulatory cell differentiation by facilitating TCR costimulation.

Plasmacytoid dendritic cells and type 1 interferon promote peripheral expansion of forkhead box protein 3+ regulatory T cells specific for the ubiquitous RNA-binding nuclear antigen La/Sjögren's syndrome (SS)-B

Convergent and divergent effects of costimulatory molecules in conventional and regulatory CD4+ T cells.

Reprogrammed FoxP3+ T regulatory cells become IL-17+ antigen-specific autoimmune effectors in vitro and in vivo.